Fang Pu, Li Xinyuan, Luo Jin Jun, Wang Hong, Yang Xiao-Feng
Center for Metabolic Disease Research, Temple University School of Medicine, Philadelphia PA, 19140, USA.
Center for Cardiovascular Research, Temple University School of Medicine, Philadelphia PA, 19140, USA ; Department of Pharmacology, Temple University School of Medicine, Philadelphia PA, 19140, USA.
Brain Disord Ther. 2013 Nov 1;2(2):109. doi: 10.4172/2168-975X.1000109.
Uric Acid (UA), historically considered as a waste of cellular metabolism, has now received increasing attention because it was found to directly participate in the pathogenesis of many human diseases including neurological disorders. On one hand, low levels of UA are detrimental to the neurons because of its induction it impairs antioxidant capacity in the cell. High levels of UA, on the other hand, lead to an inflammatory response contributing to gout or neuroprotection. In this review, we summarize this biphasic function of uric acid and highlight potential therapeutic targets to treat UA-related neurological diseases.
尿酸(UA),历史上被认为是细胞代谢的废物,现在受到越来越多的关注,因为它被发现直接参与包括神经疾病在内的许多人类疾病的发病机制。一方面,低水平的尿酸对神经元有害,因为它的诱导会损害细胞中的抗氧化能力。另一方面,高水平的尿酸会导致炎症反应,引发痛风或具有神经保护作用。在这篇综述中,我们总结了尿酸的这种双相功能,并强调了治疗与尿酸相关的神经疾病的潜在治疗靶点。